Sodium homeostasis

Definitions & Key takeaways

Sodium homeostasis refers to the regulation of sodium levels in the body. Sodium is an important electrolyte mainly found in extracellular fluid, which helps maintain fluid balance, blood pressure, nerve impulse conduction, and muscle contraction. The body regulates sodium levels through hormones that control the reabsorption of sodium in the kidneys, as well as through thirst mechanisms. Factors that stimulate sodium reabsorption include the renin-angiotensin-aldosterone system, ADH, and the sympathetic nervous system. Factors that stimulate sodium excretion include PTH, and peptides like ANP. An imbalance in sodium levels can lead to health problems such as edema, hyponatremia, and hypernatremia.

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Introduction0:00–0:42

Sodium is a positive ion or a cat ion noted with N A. Most of the sodium in our body is located outside the cells in the extracellular fluid or ECF for short, in the extracellular fluid, sodium has a concentration of about 100 and 35 mill equivalents meq per liter.
And remember that sodium concentration doesn't necessarily reflect the total amount of sodium in the body, but rather the amount of sodium relative to the amount of water in the body.
So sodium homeostasis refers to the mechanisms employed by the body to maintain a normal sodium concentration in the extracellular fluid.

Osmolality0:42–1:30

Sodium is essential in maintaining water balance as well as for nerve impulse conduction and muscle contraction. Additionally, sodium is an important determinant of the volume and osmolality of the extracellular fluid which is made up of plasma and interstitial fluid.
Now, osmolality refers to the total solute concentration in a certain amount of solvent or water by affecting plasma osmolality.
Sodium determines plasma and blood volume. So at the end of the day, it's important to maintain the sodium concentration in order to keep enough blood inside our arteries.
This blood is called the effective arterial blood volume or EBV. And it's what ends up perfusing our various organs and tissues.
Ok. Now, sodium comes from our diet.

Sodium1:30–2:04

The daily recommended sodium intake is about 2.3 g per day, which is the equivalent of a teaspoon of salt per day. Once ingested sodium is absorbed in the blood by the gi tract and travels through the bloodstream, unbound to plasma proteins.
At the other end, some sodium is eliminated from the body through Sweatt and through feces. But most of it comes out along with water as pee.
So the kidneys are the cornerstone of sodium homeostasis. See, the kidneys are made up of lots and lots of nephrons.

Nephron2:04–3:07

And each nephron is made up of a renal corpuscle and a renal tubule. The renal corpuscle in turn is made up of the glomerulus, which is a tiny clump of capillaries and Bowman's capsule surrounding it.
So blood gets to the glomerulus through the efferent arteriole, which is a branch of the renal artery and leaves the glomerulus through the efferent arterioles.
These vessels act like a coffee filter allowing everything but red blood cells and proteins to pass from the bloodstream into Bowman's capsule, which is connected to the renal tubule.
And the resulting fluid is called filtrate. Now, upon exiting the glomerulus, the efferent arterioles divide into capillaries a second time forming the peritubular vessels which wrap around the segments of the renal tubule, the proximal convoluted tubule, the U shaped loop of henley which has a descending and ascending limb.
The distal convoluted tubule and the collecting duct as filtrate passes through the renal tubule ions like sodium are filtered from the capillaries into the lumen of the tubule and reabsorbed from the lumen into the capillaries depending on the amount of sodium in the bloodstream.

Sodium Clearance3:07–3:19

Proximal Convoluted Tubule3:19–6:14

So 1st 67% of the sodium in the tubule lumen is reabsorbed in the proximal convoluted tubule or in the PCT. This segment is also permeable to water.
So, whenever a sodium molecule is reabsorbed, water is reabsorbed along with it, which is called isosmotic reabsorption.
Now, in the early PCT sodium is reabsorbed together with other molecules through three different channels. Found on the surface of tubular cells.
Sodium and glucose are reabsorbed together through the sodium glucose cotransporter. Sodium and amino acids are also reabsorbed together through the sodium amino acid cotransporter and finally phosphate and sodium are reabsorbed together through the sodium phosphate cotransporter.
An important regulatory mechanism here is parathyroid hormone or PTH, which is produced by the parathyroid glands in response to low serum calcium or high serum phosphate PTH inhibits the sodium phosphate cotransporter.
So, more sodium and phosphate are excreted. Finally, in the early PCT.
There's also a sodium hydrogen exchanger which is a cell membrane protein that reabsorbs sodium in exchange for hydrogen.
And this is mainly regulated by a molecule called angiotensin two, which is a product of the renin angiotensin aldosterone system.
Now, renin is an enzyme that's released by the kidneys in response to hypotension. In short, the way it goes is that renin stimulates angiotensinogen conversion into angiotensin.
One which is then converted into angiotensin. Two angiotensin two has many functions.
Some of which include vasoconstriction of the efferent renal arteriole and stimulating the sodium hydrogen exchanger. In turn, this increases sodium reabsorption and water reabsorption in order to bring up BP.
Second, in the late PCT sodium is still reabsorbed through the sodium hydrogen exchanger. And also along with chloride through the chloride formate exchanger.
This transporter reabsorbs chloride and secretes formate which is a negative ion derived from formic acid in the late PCT sodium and chloride can also get reabsorbed through a paracellular way, meaning that they don't use any channels, but rather they sneak between two epithelial cells and go back into the bloodstream.
If there's a lot of chloride in the tubules, then some of it will diffuse from the tubular lumen through the tubular cells.
And then in the bloodstream, losing all those negatively charged chloride ions makes the lumen more positively charged than the bloodstream, creating a lumen positive potential difference.
This potential difference will drive the paracellular reabsorption of sodium as well. OK.
Next, about 25% of the sodium is further reabsorbed in the thick ascending loop of henley or ta L for short this segment however, is impermeable to water.

Sodium-Potassium-Chloride Cotransporter6:14–7:06

So no water is reabsorbed along with the sodium in the tal sodium is reabsorbed along with potassium and chloride through the sodium potassium chloride cotransporter.
Also called NKCC two. An important regulatory mechanism here is anti diuretic hormone or ADH, which is secreted by the posterior part of the pituitary gland up in the brain in response to decreased blood volume or increased blood osmolality.
So when there are too many solutes compared to water in the blood, when secreted, this stimulates NKCC two, increasing sodium chloride and potassium reabsorption.

Distal Tubule7:06–8:05

Next, in the early distal tubule, 5% of the filtered sodium is reabsorbed and just like tal, it's impermeable to water. Here, there's a sodium chloride co transporter that reabsorbs both sodium and chloride in the late distal tubule and the collecting ducts.
The remaining 3% of filtered sodium is reabsorbed. These segments are in charge of fine tuning blood sodium concentration.
The key players here are some cells in the tubule wall called the principal cells which have epithelial sodium channels or enac for short on their surface sodium is reabsorbed by enac in response to aldosterone, which is the final product of the renin angiotensin aldosterone system, aldosterone is secreted in response to low BP and it induces the synthesis of more enac channels which allows for more sodium to be reabsorbed.
So, BP increases and just in case all that wasn't enough, there are a couple of other mechanisms acting on the kidneys to regulate sodium concentration and keep EBV and BP in the normal range.

Sympathetic Nervous System8:05–8:32

First off, there's the sympathetic nervous system which activates when there's a decrease in BP and causes vasoconstriction of the afferent arterioles in the glomerulus.
Additionally, it also increases sodium reabsorption in the proximal tubule. At the other end of the spectrum, there is atriopeptin or ANP which is secreted by the atria when EBV is increased.

Atriopeptin (ANP)8:32–10:09

So, high BP, ANP causes vasodilation of the afferent arterioles and vasoconstriction of the efferent arterioles which increases the glomerular filtration rate.
So more blood is filtered by the glomerulus A and P also inhibits en ac channels in the late distal tubule and collecting ducts, decreasing sodium reabsorption.
So, more sodium and water are eliminated, decreasing BP. Other peptides similar to an P include uro dilat which is secreted by the kidneys themselves and the brain natriuretic peptide or BNP, which is secreted by the brain and the cardiac ventricular cells.
They are also secreted in response to high BP and act just like AP to bring it down, but they have a lower intensity. Let's finish off with two examples.
When an individual has a diet high in sodium, the extracellular fluid and in turn the eab and BP increase. So, atriopeptin is secreted and the kidneys excrete more sodium and water lowering BP.
Alternatively, on a low sodium diet, the extracellular fluid eab v and BP are low in response. The sympathetic nervous system and the renin angiotensin aldosterone system activate increasing sodium and water reabsorption to bring BP back up.
All right, as a quick recap sodium is a cat ion that's mostly in the extracellular fluid and is essential for maintaining water balance as well as nerve impulse conduction and muscle contraction.

Review10:09–11:16

Sodium is filtered across the glomerular capillaries in the PCT. 67% of the filtered sodium is reabsorbed through the sodium glucose co transporter.
The sodium amino acid co transporter, the sodium phosphate cotransporter and the sodium hydrogen exchanger in the tal. About 25% of the sodium is reabsorbed through the sodium potassium chloride or NKCC two cotransporter in the early distal tubule.
5% of the filtered sodium is reabsorbed through a sodium chloride cotransporter. The late distal tubule and the collecting ducts reabsorb about 3% of the filtered sodium through epithelial sodium channels or en A CS factors that stimulate sodium reabsorption include the renin angiotensin aldosterone system ADH.
And the sympathetic nervous system factors that stimulate sodium excretion include pth and peptides like AP